Agent for enhancing environmental stress tolerance of plants and method for enhancing environmental stress tolerance

Abstract

To provide an agent for enhancing environmental stress tolerance that effectively improves the environmental stress tolerance of plants.SOLUTION: An agent for enhancing environmental stress tolerance of plants comprises, as an active ingredient, a compound represented by formula (I) in the figure or a tautomer thereof, or an agriculturally acceptable salt of them. (In formula (I), R1 and R2 each independently represent a hydrogen atom or an alkyl group having 1 to 4 carbon atoms, and R3 to R5 each independently represent an alkyl group having 1 to 4 carbon atoms.)SELECTED DRAWING: None

Description

[Technical Field]

[0001] The present invention relates to an agent for improving environmental stress tolerance in plants and a method for improving environmental stress tolerance in plants. [Background technology]

[0002] Environmental stresses such as global warming, drought, and salt damage adversely affect plant survival, causing serious damage to agriculture. Because eliminating environmental stresses is difficult or expensive, there has been a need for chemicals that can improve environmental stress tolerance in a wide range of plants.

[0003] Here, ergothioneine is known as a compound that can affect plant growth.

[0004] Patent Document 1 discloses a fertilizer containing ergothioneine and a culture of a microorganism capable of biosynthesizing ergothioneine.

[0005] Patent Document 2 reports that applying ergothioneine alone to plants promotes plant growth or increases yield.

[0006] Patent Document 3 reports that nitrogenase activity is improved by applying a microbial extract containing ergothioneine as a fertilizer.

[0007] Furthermore, Patent Documents 4 and 5 report that applying glycine betaine to plants controls stress and related conditions in the plants and promotes plant growth. [Prior art documents] [Patent documents]

[0008] [Patent Document 1] Japanese Patent Application Publication No. 2018-130091 [Patent Document 2] Patent Application No. 2019-128636 [Patent Document 3] European Patent Application Publication No. 3696154 [Patent Document 4] International Publication No. 96 / 14749 [Patent Document 5] International Publication No. 96 / 23413 Summary of the Invention [Problem to be solved by the invention]

[0009] As mentioned above, various agents for improving environmental stress tolerance have been developed, but there is still a need for agents for improving environmental stress tolerance that exhibit even better effects. However, Patent Documents 1, 2, and 3 do not clearly state the effect of improving environmental stress tolerance in plants. Patent Documents 4 and 5 also describe 2-mercaptohistidine betaine (ergothioneine) in addition to glycine betaine, but there are no examples for ergothioneine, and its effects have not been confirmed.

[0010] Therefore, an object of one aspect of the present invention is to provide an environmental stress tolerance improver and a method for improving environmental stress tolerance that can effectively improve the environmental stress tolerance of plants. [Means for solving the problem]

[0011] In order to solve the above-mentioned problems, one embodiment of the present invention provides an agent for improving environmental stress tolerance in plants, which comprises, as an active ingredient, a compound represented by the following formula (I) or a tautomer thereof, or an agriculturally acceptable salt thereof: [ka] (In formula (I), R 1 and R 2 each independently represents a hydrogen atom or an alkyl group having 1 to 4 carbon atoms, and R 3 ~R 5 each independently represents an alkyl group having 1 to 4 carbon atoms).

[0012] In order to solve the above-mentioned problems, a method for improving environmental stress tolerance in a plant according to one aspect of the present invention comprises treating a plant with the above-mentioned environmental stress tolerance improver. [Effects of the Invention]

[0013] According to one aspect of the present invention, it is possible to provide an environmental stress tolerance improver and a method for improving environmental stress tolerance that can effectively improve the environmental stress tolerance of a plant. DETAILED DESCRIPTION OF THE INVENTION

[0014] [Environmental stress tolerance improver] (active ingredient) The environmental stress tolerance improver according to this embodiment contains, as an active ingredient, a compound represented by the following formula (I) (hereinafter simply referred to as "compound (I)") or a tautomer thereof, or an agriculturally acceptable salt thereof: [ka] In formula (I), R 1 and R 2 R independently represents a hydrogen atom or an alkyl group having 1 to 4 carbon atoms. 3 ~R 5 are independently an alkyl group having 1 to 4 carbon atoms.

[0015] The alkyl group may be straight-chain or branched, ie, methyl, ethyl, propyl, isopropyl, butyl, isobutyl, sec-butyl or tert-butyl.

[0016] R 1 and R 2 At least one of R is preferably a hydrogen atom, and more preferably both are hydrogen atoms. 1 and R 2When is an alkyl group, it is preferably a methyl group, an ethyl group, or a propyl group, more preferably a methyl group or an ethyl group, and even more preferably a methyl group.

[0017] R 3 ~R 5 are preferably independently a methyl group, an ethyl group, or a propyl group, more preferably a methyl group or an ethyl group, and even more preferably a methyl group. 3 ~R 5 Preferably, at least one of the groups is a methyl group, more preferably at least two of the groups are methyl groups, and even more preferably all of the groups are methyl groups.

[0018] "Tautomer thereof" refers to a tautomer of Compound (I). Compound (I) contains R 1 and R 2 When at least one of R is a hydrogen atom, tautomers exist. 2 When R is a hydrogen atom, a compound represented by the following formula (II) (hereinafter simply referred to as "compound (II)") may exist as a tautomer. 1 When is a hydrogen atom, a compound represented by the following formula (III) (hereinafter simply referred to as "compound (III)") may exist as a tautomer. Hereinafter, compound (II) and compound (III) will be collectively referred to simply as "tautomers." [ka] In formulas (II) and (III), R 1 ~R 5 is R in formula (I) 1 ~R 5 is the same as

[0019] A preferred compound as compound (I) or a tautomer thereof is specifically ergothioneine, and more preferably L-(+)-ergothioneine.

[0020] These compounds may be commercially available or synthesized by techniques well known to those skilled in the art, such as the methods described in Patent Document JP-A-2013-506706 or JP-A-2006-160748. Ergothioneine is also known to be produced by bacteria and fungi. Examples of production methods using such microorganisms include those described in Patent Documents JP-A-2012-105618, JP-A-2014-223051, WO2016 / 104437, WO2016 / 121285, WO2015 / 168112, and WO2017 / 150304. Ergothioneine may be obtained from a culture containing ergothioneine obtained from these microorganisms, or it may be concentrated or purified before use.

[0021] "Agriculturally acceptable" generally means something that is safe, non-toxic, and not biologically or otherwise undesirable, and is acceptable for agricultural use, particularly for improving environmental stress tolerance in plants.

[0022] An "agriculturally acceptable salt" of Compound (I) or its tautomer means an agriculturally acceptable salt as defined above that provides the functions and effects of Compound (I) or its tautomer. Examples of such salts include hydrates, solvates, acid addition salts, salts formed when an acidic proton present in Compound (I) or its tautomer is substituted with a metal ion, and salts formed when the acidic proton is coordinated with an organic or inorganic base.

[0023] Acid addition salts may be formed with inorganic or organic acids, including hydrochloric, hydrobromic, sulfuric, nitric, and phosphoric acids. Organic acids include acetic, benzenesulfonic, benzoic, camphorsulfonic, citric, ethanesulfonic, fumaric, glucoheptonic, gluconic, glutamic, glycolic, hydroxynaphthoic, 2-hydroxyethanesulfonic, lactic, maleic, malic, mandelic, methanesulfonic, muconic, 2-naphthalenesulfonic, propionic, salicylic, succinic, dibenzoyl-L-tartaric, tartaric, p-toluenesulfonic, trimethylacetic, and trifluoroacetic acids.

[0024] Examples of metal ions that can be substituted for the acidic protons present in compound (I) or its tautomers include alkali metal ions, alkaline earth metal ions, and aluminum ions.

[0025] Examples of organic bases capable of coordinating with the acidic protons present in Compound (I) or its tautomers include diethanolamine, ethanolamine, N-methylglucamine, triethanolamine, tromethamine, etc. Examples of inorganic bases include aluminum hydroxide, calcium hydroxide, potassium hydroxide, sodium carbonate, sodium hydroxide, etc.

[0026] The environmental stress tolerance improver of this embodiment contains compound (I) or a tautomer thereof, or an agriculturally acceptable salt thereof as an active ingredient, and thus plants treated with the agent have improved tolerance to environmental stress compared to plants not treated with the agent.

[0027] In this specification, "enhancing tolerance to environmental stress" refers to the suppression of physiological disorders caused by environmental stress in plants treated with the environmental stress tolerance improver of this embodiment compared to plants not treated with the agent.

[0028] An example of an "indicator of suppression of physiological disorders caused by environmental stress" is the environmental stress suppression rate. The "environmental stress suppression rate" refers to the rate at which physiological disorders occurring in a plant after growing for a predetermined period of time under an environmental stressed environment are suppressed by treating the plant with an environmental stress tolerance improver according to an embodiment, compared to a plant that is not treated with the agent. For example, if the physiological disorders occurring in a plant under an environmental stressed environment without treatment is taken as 100%, and the physiological disorders occurring in a plant treated with the agent are taken as 20%, then the environmental stress suppression rate is 80%. With regard to the "environmental stress suppression rate," "enhancing tolerance to environmental stress" means that the environmental stress suppression rate is high.

[0029] Examples of "indicators of physiological disorders" include, for example, withering, chlorosis (whitening or yellowing), necrosis (necrosis), and wilting in plants, and for example, withering, chlorosis (whitening or yellowing), necrosis (necrosis), and wilting in leaves, but are not limited to these, and examples include decreases in plant height, root length, number of flowers, number of fruits, and seed yield.

[0030] An example of "plant mortality" is the ratio of the number of plants that have died after growing the plants under specified conditions for a specified period of time to the number of plants tested; for example, if 80 plants have died after growing 100 plants under specified conditions for a specified period of time, the mortality rate is 80%. With regard to "plant mortality," "enhanced resistance to environmental stress" means that plants treated with the environmental stress tolerance improver according to this embodiment have a lower mortality rate in an environment where environmental stress is applied, compared to plants that have not been treated with the agent.

[0031] An example of "leaf mortality" is the ratio of the number of leaves that have died after a test plant has been grown for a specified period under specified conditions to the total number of leaves on the plant; for example, if a plant has been grown for a specified period under specified conditions and 8 of 10 leaves have died, the leaf mortality is 80%. With regard to "leaf mortality," "enhanced resistance to environmental stress" means that plants treated with the environmental stress tolerance improver according to this embodiment have a lower mortality in an environment where environmental stress is imposed, compared to plants that have not been treated with the agent.

[0032] An example of the "leaf bleaching rate" is the ratio of the number of bleached leaves after a test plant has been grown for a specified period under specified conditions to the total number of leaves on the plant; for example, if 8 out of 10 leaves have bleached after a plant has been grown for a specified period under specified conditions, the leaf bleaching rate is 80%. With regard to the "leaf bleaching rate," the phrase "improving resistance to environmental stress" means that a plant treated with the environmental stress tolerance improver according to this embodiment has a lower bleaching rate in an environment where environmental stress is applied, compared to a plant that has not been treated with the agent.

[0033] An example of "leaf necrosis rate" is the ratio of necrotic leaf area to the total leaf area of ​​the test plant after the plant has been grown under specified conditions for a specified period of time. For example, the ratio of necrotic leaf area to the total leaf area of ​​the test plant after the plant has been grown under specified conditions for a specified period of time is 2 Of which, 80cm 2 When all the leaves are necrotic, the leaf necrosis rate is 80%. With regard to the "leaf necrosis rate," the phrase "enhanced tolerance to environmental stress" means that a plant treated with the environmental stress tolerance improver according to this embodiment has a lower necrosis rate under an environment where environmental stress is applied, compared to a plant not treated with the agent.

[0034] An example of the "leaf wilting rate" is the ratio of the number of leaves that have wilted after a test plant has been grown for a specified period under specified conditions to the total number of leaves on the plant; for example, if 8 out of 10 leaves have wilted after a plant has been grown for a specified period under specified conditions, the leaf wilting rate is 80%. With regard to the "leaf wilting rate," the phrase "improving resistance to environmental stress" means that a plant treated with the environmental stress tolerance improver according to this embodiment has a lower wilting rate in an environment where environmental stress is applied, compared to a plant that has not been treated with the agent.

[0035] With respect to "plant height," as another example, "enhanced tolerance to environmental stress" means that a plant treated with the environmental stress tolerance improver according to this embodiment has a higher plant height under an environmental stress environment than a plant not treated with the agent. With respect to "root length," as another example, "enhanced tolerance to environmental stress" means that a plant treated with the environmental stress tolerance improver according to this embodiment has a longer root length under an environmental stress environment than a plant not treated with the agent. With respect to "number of flowers," as another example, "enhanced tolerance to environmental stress" means that a plant treated with the environmental stress tolerance improver according to this embodiment has a greater number of flowers under an environmental stress environment than a plant not treated with the agent. With respect to "number of fruits," as another example, "enhanced tolerance to environmental stress" means that a plant treated with the environmental stress tolerance improver according to this embodiment has a greater number of fruits under an environmental stress environment than a plant not treated with the agent. Furthermore, in regard to another example, "seed yield," "tolerance to environmental stress is improved" means that a plant treated with the environmental stress tolerance improver of this embodiment will have a higher seed yield under an environment where environmental stress is imposed, compared to a plant not treated with the agent.

[0036] Among these, a preferred embodiment is an agent for improving environmental stress tolerance for suppressing withering, chlorosis (whitening or yellowing), necrosis (necrosis), or wilting of plants or leaves due to environmental stress.

[0037] As used herein, "environmental stress" refers to environmental factors that plants may be subjected to that inhibit normal growth, such as high temperature stress, low temperature stress, freezing stress, salt stress, excess nutrient stress, drought stress, excess water stress, ultraviolet stress, weak light stress, and strong light stress.

[0038] These factors are basically conditions that make normal growth difficult without treatment with the environmental stress tolerance improver according to this embodiment. Normal growth here refers to the level of growth in a state where these factors are not present and where the plant is not treated with the environmental stress tolerance improver according to this embodiment. Difficulty in normal growth also includes cases where growth is difficult, as well as cases where the level of growth is poorer than normal growth.

[0039] The environmental stress tolerance improver according to this embodiment preferably contains Compound (I) or an agriculturally acceptable salt thereof as an active ingredient. The environmental stress tolerance improver according to this embodiment may contain, as active ingredients, a plurality of compounds selected from Compound (I) and its tautomers or agriculturally acceptable salts thereof.

[0040] Generally, in a solution, Compound (I) and Compound (II) or Compound (III) may exist in equilibrium. The ratio of Compound (I) to Compound (II) or Compound (III) may vary depending on the solvent, temperature, pH, or the like.

[0041] (Applicable to) The environmental stress tolerance improver in this embodiment generally exhibits an effect of improving environmental stress tolerance in all plants, and examples of applicable plants include the following. Gramineae such as rice, wheat, barley, rye, oats, triticale (triticale), corn, sorghum, sugarcane, lawn grass, bentgrass, Bermuda grass, fescue, and ryegrass; Fabaceae such as soybean, peanut, kidney bean, pea, adzuki bean, and alfalfa; Convolvulaceae such as sweet potato; Solanaceae such as chili pepper, bell pepper, tomato, eggplant, potato, and tobacco; Polygonaceae such as buckwheat; Asteraceae such as sunflower; Araliaceae such as ginseng; Brassicaceae such as rapeseed, broccoli, Chinese cabbage, turnip, cabbage, arugula, radish, and radish; Chenopodiaceae such as sugar beet; Malvaceae such as cotton; Rubiaceae such as coffee plants; Sterculiaceae such as kaosi (green onions), Theaceae such as tea, Cucurbitaceae such as watermelon, melon, cucumber and pumpkin, Liliaceae such as onion, leek and garlic, Rosaceae such as strawberry, apple, almond, apricot, plum, cherry, plum, peach and pear, Umbelliaceae such as carrot, Araceae such as taro, Anacardiaceae such as mango, Bromeliaceae such as pineapple, Papaya family such as papaya, Ebenaceae such as persimmon, Ericaceae such as blueberry, Juglandaceae such as pecan, Musaceae such as banana, Oleaceae such as olive, Palm family such as coconut and date palm, Rutaceae such as mandarin orange, orange, grapefruit and lemon, Vitaceae such as grapes, Flowers and ornamental plants, trees other than fruit trees and other ornamental plants.

[0042] Also included are wild plants, plant cultivars, plants and plant cultivars obtained by conventional biological breeding such as crossbreeding or protoplast fusion, and genetically modified plants and plant cultivars obtained by genetic engineering. Examples of genetically modified plants and plant cultivars include herbicide-resistant crops, pest-resistant crops incorporating genes that produce insecticidal proteins, disease-resistant crops incorporating genes that produce disease-resistance inducers, crops with improved eating quality, crops with improved yield, crops with improved storability, and crops with improved yield. Genetically modified plant cultivars approved in various countries include those stored in the database of the International Society for the Advancement of Agricultural Sciences (ISAAA). Specifically: AgriSure, AgriSure 3000GT, AgriSure 3122 EZ Refuge, AgriSure 3122 Refuge Renew, AgriSure Artesian 3030A, AgriSure Artesian 3011A, AgriSure Duracade, AgriSure Duracade 5222 EZ Refuge, AgriSure GT, AgriSure GT / CB / LL, AgriSure RW, AgriSure Viptera 3110, AgriSure Viptera 3111, AgriSure Viptera 3220 EZ Refuge, AgriSure Viptera 3220 Refuge Renew, BiteGard, Bollgard, Bollgard II, Bollgard II / Roundup Ready, Bollgard 3 XtendFlex Cotton, Bollgard Cotton, Bollgard / Roundup Ready Cotton, Bt, Bt / BXN Cotton, Bt Maize, BtXtra, BXN, BXN Canola, BXN Cotton, Clearfield, DroughtGard, Enlist, Enlist Cotton, Enlist WideStrike 3 Cotton, Genuity, Genuity Bollgard II XtendFlex, Genuity Intacta RR2 Pro, GenuitySmartStax、Genuity SmartStax RIB Complete、Genuity VT Double Pro、Genuity VT Double Pro RIB Complete、Genuity VT Triple Pro、Genuity VT Triple Pro RIB Complete、GlyTol、GlyTol Cotton、Herculex、Herculex 1、Herculex RW、Herculex XTRA、IMI、IMI Canola、InVigor、KnockOut、Liberty Link、Liberty Link Conola、Liberty Link cotton、NatureGard、Newleaf、Nucotn、Optimum、Optimum AcreMax、Optimum AcreMax I、Optimum AcreMax-R、Optimum AcreMax RW、Optimum AcreMax RW-R、Optimum AcreMax Xtra-R、Optimum AcreMax Xtreme-R、Optimum AcreMax Xtreme、Optimum Intrasect、Optimum Intrasect Xtra、Optimum Intrasect Xtreme、Optimum Leptra、Optimum TRIsect、Poast Compatible、Powercore、Powercore Corn、Powercore Corn Refuge Advanced、Protecta、Roundup Ready、Roundup Ready 2、Roundup Ready Conola、Roundup Ready Cotton、Roundup Ready Xtend、Roundup Ready / YieldGard、RR Flex / Bollgard II、SCS、SmartStax、SmartStax Refuge Advanced、StarLink、Twinlink、VipCot、VipCot Cotton、WideStrike、WideStrike 3、YieldGard、YieldGard Corn Borner、YieldGard Rootworm、YieldGard PlusおよびYieldGardExamples include those that include registered trademarks such as VT Triple.

[0043] (formulation) The environmental stress tolerance improver in this embodiment is generally formulated by mixing the active ingredient, Compound (I), or a tautomer thereof, or a mixture thereof with a carrier, a surfactant, and other formulation adjuvants, and then using the formulation in various forms such as dusts, granules, powders, wettable powders, water-soluble powders, emulsions, liquids, oils, aerosols, microcapsules, pastes, liniments, fumigants, fumigants, and trace dusts.

[0044] Carriers used as formulation adjuvants include solid carriers and liquid carriers. Solid carriers are used as powder carriers and granular carriers, and include, for example, minerals such as clay, talc, diatomaceous earth, zeolite (boiling stone), montmorillonite, bentonite, kaolinite, kaolin, pyrophyllite, rosewood, acid clay, activated clay, attapulgite, attapulgus clay, limestone, calcite, marble, vermiculite, perlite, pumice, silica stone, silica sand, sericite (sericite), and pottery stone; synthetic organic substances such as urea; salts such as calcium carbonate, sodium carbonate, magnesium carbonate, sodium sulfate, ammonium sulfate, potassium chloride, slaked lime, and sodium bicarbonate; amorphous silica (white Examples of suitable carriers include synthetic inorganic materials such as carbon, fumed silica, etc. and titanium dioxide; plant-based carriers such as wood flour, corn stalks (cobs), walnut shells (nut husks), fruit kernels, rice husks, coconut shells, sawdust, bran, soybean flour, powdered cellulose, starch, dextrin, and sugars (lactose, sucrose, etc.); and various polymeric carriers such as cross-linked lignin, cationic gels, gelatin that gels with heat or polyvalent metal salts, water-soluble polymer gels (agar, etc.), chlorinated polyethylene, chlorinated polypropylene, polyvinyl acetate, polyvinyl chloride, ethylene / vinyl acetate copolymers, and urea / aldehyde resins.

[0045] Examples of liquid carriers include aliphatic solvents such as paraffins (normal paraffin, isoparaffin, naphthene); aromatic solvents such as xylene, alkylbenzene, alkylnaphthalene, and solvent naphtha; mixed solvents such as kerosene; machine oils such as refined high-boiling aliphatic hydrocarbons; alcohols such as methanol, ethanol, isopropanol, butanol, and cyclohexanol; polyhydric alcohols such as ethylene glycol, diethylene glycol, propylene glycol, dipropylene glycol, hexylene glycol, polyethylene glycol, and polypropylene glycol; polyhydric alcohol derivatives such as propylene glycol ethers; acetone, acetophenone, Examples of suitable solvents include ketones such as cyclohexanone, methylcyclohexanone, and γ-butyrolactone; esters such as fatty acid methyl esters (coconut oil fatty acid methyl esters), ethylhexyl lactate, propylene carbonate, and dibasic acid methyl esters (dimethyl succinate, dimethyl glutamate, dimethyl adipate); nitrogen-containing solvents such as N-alkylpyrrolidones and acetonitrile; sulfur-containing solvents such as dimethyl sulfoxide; oils and fats such as coconut oil, soybean oil, and rapeseed oil; amide solvents such as dimethylformamide, N,N-dimethyloctanamide, N,N-dimethyldecanamide, 5-(dimethylamino)-2-methyl-5-oxo-valeric acid methyl ester, and N-acylmorpholine solvents (CAS No. 887947-29-7, etc.); and water.

[0046] Surfactants used as formulation adjuvants include nonionic surfactants, anionic surfactants, cationic surfactants, amphoteric surfactants, silicone surfactants, fluorine-containing surfactants, and biosurfactants. Examples of nonionic surfactants include sorbitan fatty acid esters, polyoxyethylene sorbitan fatty acid esters, sucrose fatty acid esters, polyoxyethylene fatty acid esters, polyoxyethylene resin acid esters, polyoxyethylene fatty acid diesters, polyoxyethylene alkyl ethers, polyoxyethylene alkylphenyl ethers, polyoxyethylene dialkylphenyl ethers, polyoxyethylene alkylphenyl ether formalin condensates, polyoxyethylene / polyoxypropylene block polymers, alkyl polyoxyethylene / polyoxypropylene block polymer ethers, alkylphenyl polyoxyethylene / polyoxypropylene block polymer ethers, polyoxyethylene alkylamines, polyoxyethylene fatty acid amides, polyoxyethylene fatty acid bisphenyl ethers, polyoxyethylene benzylphenyl (or phenylphenyl) ethers, polyoxyethylene styrylphenyl (or phenylphenyl) ethers, polyoxyethylene castor oil, polyoxyethylene hydrogenated castor oil, and alkyl glycosides.

[0047] Examples of anionic surfactants include sulfates such as alkyl sulfate, polyoxyethylene alkyl ether sulfate, polyoxyethylene alkylphenyl ether sulfate, polyoxyethylene benzyl (or styryl) phenyl (or phenylphenyl) ether sulfate, and polyoxyethylene / polyoxypropylene block polymer sulfate; paraffin (alkane) sulfonate, α-olefin sulfonate, dialkyl sulfosuccinate, alkylbenzene sulfonate, mono- or dialkylnaphthalene sulfonate, naphthalene sulfonate-formalin condensate, alkyl diphenyl ether disulfonate, lignin sulfonate, poly Examples of suitable carboxylic acids include sulfonates such as oxyethylene alkyl phenyl ether sulfonate and polyoxyethylene alkyl ether sulfosuccinic acid half ester; carboxylates such as fatty acids, resin acids, polycarboxylic acids, alkyl ether carboxylates, alkenyl succinic acids, N-acyl amino acids, and naphthenic acids; and phosphates such as polyoxyethylene alkyl ether phosphate, polyoxyethylene mono- or dialkyl phenyl ether phosphate, polyoxyethylene benzyl (or styryl) phenyl (or phenylphenyl) ether phosphate, polyoxyethylene / polyoxypropylene block polymer phosphate, and alkyl phosphate.

[0048] Examples of cationic surfactants include salts of amines such as alkylamines and alkylpentamethylpropylenediamines; and salts of ammoniums such as alkyltrimethylammonium, methylpolyoxyethylenealkylammonium, alkylpyridinium, mono- or di-alkylmethylated ammonium, alkyldimethylbenzalkonium, and benzethonium (octylphenoxyethoxyethyldimethylbenzylammonium).

[0049] Examples of amphoteric surfactants include dialkyldiaminoethyl betaine, alkyldimethylbenzyl betaine, and lecithin (phosphatidylcholine, phosphatidylethanolamine, etc.).

[0050] Examples of silicone surfactants include trisiloxane ethoxylate.

[0051] Examples of fluorosurfactants include perfluoroalkyl carboxylates, perfluoroalkyl sulfonates, and perfluoroalkyl trimethylammonium salts.

[0052] Examples of biosurfactants include sophorolipids, rhamnolipids, trehalose lipids, mannosylalditol lipids, cellobiose lipids, glucose lipids, oligosaccharide fatty acid esters, spiculesporic acid, corynomycolic acid, agaritic acid, surfactin, cerawettin, viscosin, lykensin, arthrofactin, emulsan, and alasan.

[0053] Other pharmaceutical adjuvants include inorganic salts (sodium, potassium, etc.) used as pH adjusters; water-soluble salts such as table salt; thickeners such as xanthan gum, guar gum, carboxymethylcellulose, polyvinylpyrrolidone, carboxyvinyl polymers, acrylic polymers, polyvinyl alcohol, starch derivatives, water-soluble polymers (polysaccharides, etc.), alginic acid and its salts; disintegrating and dispersing agents such as metal stearates, sodium tripolyphosphate, and sodium hexametaphosphate; preservatives such as benzoic acid and its salts, sorbic acid and its salts, propionic acid and its salts, p-hydroxybenzoic acid, methyl p-hydroxybenzoate, and 1,2-benzothiazolin-3-one; and supplements such as Examples of suitable anti-oxidants include sodium polyphosphate, sodium polyacrylate, sodium lignosulfonate, sodium citrate, gluconate / sodium glucoheptanoate, ethylenediaminetetraacetic acid and its disodium or ammonium salts; pigments and dyes used as colorants; fluorine-based anti-foaming agents, silicone-based anti-foaming agents, ethylene oxide / propylene oxide copolymers used as anti-oxidants; phenolic antioxidants, amine-based antioxidants, sulfur-based antioxidants, phosphate-based antioxidants used as antioxidants; salicylic acid-based UV absorbers, benzophenone-based UV absorbers used as UV absorbers; quicklime, magnesium oxide used as desiccants; and spreading agents and phytotoxicity reducers.

[0054] The formulations are either used as is or diluted with a diluent such as water to a predetermined concentration. When diluted for use, the concentration of Compound (I) is preferably in the range of 0.0001 to 1% by weight. The same applies to tautomers of Compound (I).

[0055] These formulations contain 0.1 to 90% by weight, more preferably 0.2 to 50% by weight, of Compound (I) as the active ingredient. The amount of Compound (I) used is 0.005 to 50 kg, more preferably 0.03 to 30 kg, per hectare of agricultural or horticultural land, such as fields, rice paddies, orchards, and greenhouses. The same applies to tautomers of Compound (I). These concentrations and amounts vary depending on the formulation, application time, application method, application location, and target plants, and can be increased or decreased without adhering to the above ranges.

[0056] (Other active ingredients) The environmental stress tolerance improver in the present embodiment can be used in combination with other known active ingredients to enhance its performance as an environmental stress tolerance improver, or to impart an effect other than improving environmental stress tolerance. Examples of other known active ingredients include active ingredients contained in known environmental stress tolerance improvers, known plant growth regulators, fungicides, insecticides, miticides, nematicides, and herbicides.

[0057] Known active ingredients of environmental stress tolerance improvers include, for example, seaweed extract, corn extract, microalgae, mycorrhizal fungi, humic acid, fulvic acid, oxidized glutathione, L-proline, glycine betaine, 5-aminolevulinic acid, 2-hexenal, trehalose, silicic acid, nicotinic acid, acetic acid, and ethanol.

[0058] Examples of known active ingredients of plant growth regulators include aminoethoxyvinylglycine, chlormequat, chlorpropham, cyclanilide, dikegulac, daminozide, ethephon, flurprimidol, flumetralin, forchlorfenuron, gibberellin, mepiquat chloride, methylcyclopropene, benzylaminopurine, paclobutrazol, prohexadione, thidiazuron, tributyl phosphorotrithioate, trinexapac-ethyl, uniconazole, and 1-naphthalene acetate sodium. sodium, 1-naphthylacetamide, 1-methylcyclopropene, 4-CPA (4-chlorophenoxyacetic acid), MCPB (ethyl 2-methyl-4-chlorophenoxybutyrate), isoprothiolane, indolebutyric acid, ethychlozate, calcium formate, chlormequat, choline, cyanamide, dichlorprop, decyl alcohol, sorbitan trioleate, nicosulfuron, pyraflufen-ethyl, butruarin, prohydrojasmone, anicifluprine, and pendimethalin.

[0059] Suitable active ingredients for fungicide applications include, for example, inhibitors of nucleic acid synthesis metabolism, fungicides acting on the cytoskeleton and motor proteins, respiratory inhibitors, inhibitors of amino acid and protein biosynthesis, signal transduction inhibitors, inhibitors of lipid biosynthesis or transport / cell membrane structure or function, inhibitors of cell membrane sterol biosynthesis, inhibitors of cell wall biosynthesis, inhibitors of melanin biosynthesis, inducers of host plant resistance, multi-site fungicides and biopesticides / biological pesticides with multiple modes of action.

[0060] Specific examples of nucleic acid synthesis metabolic inhibitors include benalaxyl, benalaxyl M or chiralaxyl, furalaxyl, metalaxyl, metalaxyl M or mefenoxam, ofurace, oxadixyl, bupirimate, dimethirimol, ethirimol, hydroxyisoxazole, octhilinone, and oxolinic acid.

[0061] Furthermore, fungicides that act on the cytoskeleton and motor proteins include benomyl, carbendazim, fuberidazole, thiabendazole, thiophanate, thiophanate-methyl, diethofencarb, ethaboxam, pencycuron, zoxamide, fluopicolide, fluopimomide, fenamacril, metrafenone, and pyriophenone.

[0062] Respiratory inhibitors include diflumetrim, fenazaquin, tolfenpyrad, benodanil, benzovindiflupyr, bixafen, boscalid, carboxin, fenfuram, flubeneteram, fluindapyr, fluopyram, flutolanil, fluxapyroxad, furametpyr, inpirfluxam, isofetamide, isoflucipram, isopyrazam, mepronil, oxycarboxin, penflufen, penthiopyrad, pydiflumetofen, pyrapropoin, pyraziflumid, sedaxane, thifluzamide, azoxystrobin, cumoxystrobin, dimoxystrobin, enestrobin, enoxastrobin, famoxadone, and fenamide Examples of antibacterial agents include phenaminestrobin, flufenoxystrobin, fluoxastrobin, kresoxim-methyl, mandestrobin, metominostrobin, methyltetraprole, orysastrobin, picoxystrobin, pyraclostrobin, pyrametostrobin, pyroxystrobin, pyribencarb, triclopyricarb, trifloxystrobin, amisulbrom, cyazofamid, fenpicoxamide, florylpicoxamide, methallylpicoxamide, binapacryl, dinocap, fluazinam, meptyldinocap, triphenyltin acetate, triphenyltin chloride, triphenyltin hydroxide, silthiofam, and ametoctrazine.

[0063] Furthermore, examples of amino acid and protein biosynthesis inhibitors include cyprodinil, mepanipyrim, pyrimethanil, blasticidin S, kasugamycin, streptomycin, and oxytetracycline.

[0064] Furthermore, examples of signal transduction inhibitors include proquinazid, quinoxyfen, fludioxonil, chlozolinate, dimethaclon, fenpiclonil, iprodione, procymidone, and vinclozolin.

[0065] In addition, inhibitors of lipid biosynthesis or transport / cell membrane structure or function include edifenphos (EDDP), iprobenfos (IBP), isoprothiolane, pyrazophos, biphenyl, chloroneb, dicloran (CNA), etridiazole, quintozene (PCNB), tecnazene (TCNB), tolclofos-methyl, iodocarb, propamocarb, prothiocarb, tea tree extract, vegetable oil mixture (eugenol, geraniol, thymol), natamycin (pimaricin), fluoxapiprolin, and oxathiapiprolin.

[0066] Inhibitors of cell membrane sterol biosynthesis include azaconazole, bitertanol, bromuconazole, cyproconazole, difenoconazole, diniconazole, epoxiconazole, etaconazole, fenbuconazole, fluoxythioconazole, fluquinconazole, flusilazole, flutriafol, hexaconazole, imazalil, imibenconazole, ipconazole, ipfentrifluconazole, mefentrifluconazole, metconazole, myclobutanil, oxpoconazole, pefurazoate, penconazole, prochloraz, propiconazole, prothioconazole, simeconazole, tebuconazole, tetraconazole, triadimefon, triadimenol, triflumizole, triticonazole, fenarimol, nuarimol, and pyrifenoc. methyl 2-((1H-1,2,4-triazol-1-yl)methyl)-3-(4-chlorobenzyl)-2-hydroxy-1-methylcyclopentane-1-carboxylate, aldimorph, dodemorph, fenpropimorph, tridemorph, fenpropidin, piperalin, spiroxamine, fenhexamid, fenpyrazamine, pyributicarb, naftifine, and terbinafine.

[0067] Cell wall biosynthesis inhibitors include polyoxins, benthiavalicarb (benthiavalicarb isopropyl), dimethomorph, flumorph, iprovalicarb, mandipropamid, pyrimorph, and valifenalate.

[0068] Melanin biosynthesis inhibitors include fthalide, pyroquilon, tricyclazole, carpropamid, diclocymet, fenoxanil, and tolprocarb.

[0069] Resistance inducers in host plants include acibenzolar-S-methyl, probenazole, tiadinil, isotianil, laminarin, giant knotweed extract, Bacillus mycoides isolate J, Saccharomyces cerevisiae strain LAS117 cell wall, fosetyl (fosetyl-aluminum, fosetyl potassium, fosetyl sodium), phosphoric acid, phosphate salts, and diclobenthiazox.

[0070] Multi-site fungicides include ferbam, mancozeb, maneb, metiram, propineb, thiuram, zinc thiazole, zineb, ziram, ambam, anilazine, dithianon, dichlofluanid, tolylfluanid, guazatine, iminoctadine acetate, iminoctadine albesilate, copper or various copper salts (e.g., copper chloride, cupric hydroxide, copper sulfate, copper sulfate, organocopper (oxine copper), copper nonylphenolsulfonate, DBEDC, etc.), sulfur, captan, captafol, folpet, TPN (chlorothalonil), quinoxalines (quinomethionate), fluorimide, and metasulfocarb.

[0071] Biopesticides / biological pesticides with multiple modes of action include Bacillus subtilis strain AFS032321, Bacillus amyloliquefaciens strain QST713, Bacillus amyloliquefaciens strain FZB24, Bacillus amyloliquefaciens strain MBI600, Bacillus amyloliquefaciens strain D747, Bacillus amyloliquefaciens strain F727, Clonostachys rosea strain CR-7, and Gliocladium catenaratum J. 1446, Pseudomonas chlororaphis strain AFS009, Streptomyces griseovirides strain K61, Streptomyces lidicus strain WYEC108, Trichoderma atroviride strain I-1237, Trichoderma atroviride strain LU132, Trichoderma atroviride strain SC1, Trichoderma asperellum strain T34, Swaingrea glutinosa, and extracts from cotyledons of lupin seedlings.

[0072] Other compounds used as fungicides include chlorinconazid, seboxylamine, flumethylsulfolim, flufenoxadiazam, cyflufenamid, cymoxanil, diclomedine, dipimethitron, dodine, fenitropan, ferimzone, flusulfamide, flutianil, harpin, inorganic salts (bicarbonates (sodium bicarbonate, potassium bicarbonate), potassium carbonate), ipflufenoquin, quinoprol, natural products, machine oil, organic oil, picarbutrazox, pyridaclomethyl, quinofumelin, tebufloquine, tecloftalam (bactericide), triazoxide, validamycin, aminopyrifen, and shiitake mushroom mycelium extract.

[0073] Suitable active ingredients for insecticide use include, for example, acetylcholinesterase (AChE) inhibitors, GABAergic chloride channel blockers, sodium channel modulators, nicotinic acetylcholine receptor (nAChR) competitive modulators, nicotinic acetylcholine receptor (nAChR) allosteric modulators, glutamate-gated chloride channel (GluCl) allosteric modulators, juvenile hormone analogs, other non-specific (multi-site) inhibitors, chordotonal organ TRPV channel modulators, mite growth inhibitors acting on CHS1, microbial-derived insect midgut membrane disruptors, mitochondrial ATP synthase inhibitors, oxidative phosphorylation uncouplers that disrupt the proton gradient, nicotine These include nAChR channel blockers, chitin biosynthesis inhibitors acting on CHS1, chitin biosynthesis inhibitors (type 1), ecdysone receptor agonists, octopamine receptor agonists, mitochondrial electron transport chain complex III inhibitors, mitochondrial electron transport chain complex I inhibitors (METI), voltage-dependent sodium channel blockers, acetyl-CoA carboxylase inhibitors, mitochondrial electron transport chain complex IV inhibitors, mitochondrial electron transport chain complex II inhibitors, ryanodine receptor modulators, chordotonal organ modulators, GABA-gated chloride ion channel allosteric modulators, and baculoviruses.

[0074] Acetylcholinesterase (AChE) inhibitors include alanycarb, aldicarb, bendiocarb, benfuracarb, butocarboxim, butoxycarboxim, NAC (carbaryl), carbofuran, carbosulfan, ethiofencarb, BPMC (fenobucarb), fenothiocarb, formetanate, furathiocarb, MIPC (isoprocarb), methiocarb, methomyl, MTMC (metolcarb), oxamyl, pirimicarb, PHC (propoxur), thiodicarb, thiofanox, triazamate, trimethacarb, XMC, MPMC (xylylcarb), Acephate, azamethiphos, azinphos-ethyl, azinphos-methyl, cadusafos, chlorethoxyphos, CVP (chlorfenvinphos), chlormephos, chlorpyrifos, chlorpyrifos-methyl, coumaphos, CYAP (cyanophos), demeton-S-methyl, diazinon, DDVP (dichlorvos), dicrotophos, dimethoate, dimethylvinphos, ethylthiometon (disulfoton), EPN, ethion, ethoprophos, fenflur, fenamiphos, MEP (fenitrothion), MPP (fenthion), fosthiazate, heptenophos, imicyaphos, isofenphos, isopropyl O-(methoxyaminothiophosphoryl) salicylate, isoxathion, malathion, mecarbam, methamidophos, DMTP (methidathion), mevinphos, monocrotophos, BRP (naled), omethoate, oxydemeton methyl, parathion, methyl parathion (parathion methyl), PAP (phenthoate), phorate, phosalone, PMP (phosmet), phosphamidon, phoxim, pirimiphos methyl, profenofos, propetamphos, prothiofos, pyraclofos, pyridaphenthion, quinalphos, sulfotep, tebupirimfos, temephos, terbufos, CVMP (tetrachlorvinphos), thiometon, triazophos, DEP (trichlorfon), and vamidothion.

[0075] GABA-gated chloride ion channel blockers include chlordane, benzoepine (endosulfan), dienochlor, ethiprole, fipronil, pyriprole, and nicofluprole.

[0076] Sodium channel modulators include acrinathrin, allethrin (allethrin, d-cis-trans-, d-trans-isomers), bifenthrin, bioallethrin (bioallethrin, S-cyclopentenyl-isomer), bioresmethrin, chloroprallethrin, chlorfenthrin, cycloprothrin, cyfluthrin (cyfluthrin, β-isomer), cyhalothrin (cyhalothrin, λ-, γ-isomers), cypermethrin (cypermethrin, α-, β-, θ-, ζ-isomers), cyphenothrin [(1R)-trans isomer], deltamethrin, dimefluthrin, empenthrin [(EZ)-(1R)-isomer], esfenvalerate, etofenprox, and phenothrin. Examples of pesticides include ampropathrin, fenvalerate, flubrocythrinate, flucythrinate, flumethrin, fluvalinate (τ-fluvalinate), halfenprox, imiprothrin, kadesrin, metofluthrin, momfluorothrin, epsilon metofluthrin, epsilon momfluorothrin, permethrin, phenothrin [(1R)-trans isomer], prallethrin, profluthrin, pyrethrins, resmethrin, silafluofen, tefluthrin, phthalthrin (tetramethrin), tetramethrin [(1R)-isomer], tralomethrin, transfluthrin, DDT, methoxychlor, aldrin, dieldrin, and lindane (lindane).

[0077] Nicotinic acetylcholine receptor (nAChR) competitive modulators include acetamiprid, clothianidin, dinotefuran, imidacloprid, nitenpyram, thiacloprid, thiamethoxam, nicotine sulfate (nicotine), sulfoxaflor, flupyradifurone, dichloromezothiaz, phenmezodithiaz, and triflumezopyrim.

[0078] Nicotinic acetylcholine receptor (nAChR) allosteric modulators include spinetoram, spinosad, flupirimine, and GS-omega / kappa HXTX-Hv1a peptide.

[0079] Glutamate-gated chloride channel (GluCl) allosteric modulators include abamectin, emamectin benzoate, lepimectin, and milbemectin.

[0080] Juvenile hormone mimetics include hydroprene, kinoprene, methoprene, fenoxycarb, and pyriproxyfen.

[0081] Other nonspecific (multi-site) inhibitors include methyl bromide, other alkyl halides, chloropicrin, sodium aluminum fluoride, sulfuryl fluoride, borax, boric acid, disodium octaborate, sodium metaborate, tartar emetic, dazomet, metam ammonium salt, metam sodium salt, and methyl isothiocyanate.

[0082] Chordotonal TRPV channel modulators include pymetrozine, pyrifluquinazone, and afidopiropen.

[0083] Mite growth inhibitors that act on CHS1 include clofentezine, diflobidazine, hexythiazox, and etoxazole.

[0084] Microbial agents that disrupt the insect midgut membrane include Bacillus thuringiensis subsp. israelensis, Bacillus thuringiensis subsp. aizawai, Bacillus thuringiensis subsp. kurstaki, Bacillus thuringiensis subsp. tenebrionis, proteins found in Bt crops (Cry1Ab, Cry1Ac, Cry1Fa, Cry1A.105, Cry2Ab, Vip3A, mCry3A, Cry3Bb, Cry34Ab1 / Cry35Ab1), and Bacillus sphaericus.

[0085] Mitochondrial ATP synthase inhibitors include diafenthiuron, azocyclotin, tricyclohexyltin hydroxide (cyhexatin), fenbutatin oxide, BPPS (propargite), and tetradifon.

[0086] Oxidative phosphorylation uncouplers that disrupt the proton gradient include chlorfenapyr, DNOC, and sulfluramide.

[0087] Nicotinic acetylcholine receptor (nAChR) channel blockers include bensultap, cartap hydrochloride, thiocyclam, thiosultap sodium salt, and monosultap.

[0088] Chitin biosynthesis inhibitors that act on CHS1 include bistrifluron, chlorfluazuron, diflubenzuron, flucycloxuron, flufenoxuron, hexaflumuron, lufenuron, novaluron, noviflumuron, teflubenzuron, and triflumuron.

[0089] Chitin biosynthesis inhibitors (type 1) include buprofezin.

[0090] Molting inhibitors (Diptera) include cyromazine.

[0091] Molting hormone (ecdysone) receptor agonists include chromafenozide, halofenozide, methoxyfenozide, and tebufenozide.

[0092] Octopamine receptor agonists include amitraz.

[0093] Mitochondrial electron transport chain complex III inhibitors include hydramethylnon, acequinocyl, fluacrypyrim, flupiroxystrobin, and bifenazate.

[0094] Mitochondrial electron transport chain complex I inhibitors (METI) include fenazaquin, fenpyroximate, pyridaben, pyrimidifen, tebufenpyrad, tolfenpyrad, and delis (rotenone).

[0095] Voltage-gated sodium channel blockers include indoxacarb and metaflumizone.

[0096] Acetyl-CoA carboxylase inhibitors include spirodiclofen, spiromesifen, spiropydione, spidoxamat, spirobudifen, and spirotetramat.

[0097] Mitochondrial electron transport chain complex IV inhibitors include aluminum phosphide, calcium phosphide, hydrogen phosphide, zinc phosphide, hydrocyanic acid (calcium cyanide, sodium cyanide), and potassium cyanide.

[0098] Mitochondrial electron transport chain complex II inhibitors include cyenopyrafen, cetopyrafen, cyflumetofen, piflubumid, and cyclobutrifluram.

[0099] Ryanodine receptor modulators include chlorantraniliprole, cyantraniliprole, cyclaniliprole, flubendiamide, tetraniliprole, fluchlordiniliprole, thiolanthraniliprole, tetrachlorantraniliprole, cyhalodiamide, and ciprofuranilide.

[0100] Chordotonal organ modulators include flonicamide and the like.

[0101] GABA-gated chloride channel allosteric modulators include broflanilide, fluxametamide, and isocycloceram.

[0102] Examples of baculoviruses include the codling moth Cydia pomonella GV, the false codling moth Thaumatotibia leucotreta GV, the velvet bean caterpillar Anticarsis gemmatalis MNPV, and the cotton bollworm Helicoverpa armigera NPV.

[0103] Other insecticides, acaricides, and nematicides include azadirachtin, benzomate (benzoximate), phenisobromorate (bromopropylate), quinoxalines (quinomethionate), Kelthane (dicofol), lime sulfur, mancozeb, pyridalyl, sulfur, acinonapyr, amidoflumet, benzpyrimoxane, fluazaindolizine, fluensulfone, fluhexafon, flupentiofenox, flometoquin, metaldehyde, cyclopyrazoflurane, dinpropylpyridaz, trifluenfuronate, indazapiroxamet, sulfiflumin, and burkholder. These include: Ria spp., Wolbachia pipientis (Zap), Atractylodes macrocarpa extract, glycerin or propanediol-containing fatty acid monoesters, neem oil, machine oil, rapeseed oil, formulated oil, starch, reduced starch saccharification product, sodium oleate, ferric phosphate, nemadectin, Beauveria bassiana strain, Metarhizium anisopria strain (F52), Paecilomyces fumosoroseus apopka strain (97), diatomaceous earth, DCIP (dichlorodiisopropyl ether), DD (1,3-dichloropropene), levamisole hydrochloride, morantel tartrate, and tioxazafen.

[0104] Examples of active ingredients suitable for herbicide applications include acetolactate synthase (ALS) inhibitor compounds, amino acid compounds, cyclohexanedione compounds, acetamide compounds, bipyridylium compounds, allyloxyphenoxypropionic acid compounds, carbamate compounds, pyridine compounds, urea compounds, dinitroaniline compounds, protoporphyrinogen oxidase (PPO) inhibitor compounds, phenoxyacetic acid compounds, hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor compounds, and triazine compounds.

[0105] Acetolactate synthesis (ALS) inhibitor compounds include imazamethabenz and imazamethabenz-methyl, imazamox, imazapic, imazapyr, imazaquin, imazethapyr, amidosulfuron, azimsulfuron, bensulfuron and bensulfuron-methyl, chlorimuron and chlorimuron-methyl, chlorimuron-ethyl, chlorsulfuron, cinosulfuron, cyclosulfamuron, ethametsulfuron and ethametsulfuron-methyl, ethametsulfuron-ethyl, ... Xysulfuron, flazasulfuron, flucetosulfuron, flupyrsulfuron, flupyrsulfuron methyl and its salts, foramsulfuron, halosulfuron, halosulfuron methyl, imazosulfuron, iodosulfuron and its salts, iodosulfuron methyl and its salts, mesosulfuron, mesosulfuron methyl, metazosulfuron, metsulfuron, metsulfuron methyl, nicosulfuron, oxasulfuron, primisulfuron, primisulfuron Examples include furon methyl, propyrisulfuron, prosulfuron, pyrazosulfuron, pyrazosulfuron ethyl, rimsulfuron, sulfometuron, sulfometuron methyl, sulfosulfuron, thifensulfuron, thifensulfuron methyl, triasulfuron, tribenuron, tribenuron methyl, trifloxysulfuron and its salts, triflusulfuron, triflusulfuron methyl, tritosulfuron, imizamethabenz methyl, bispyribac-sodium, cloransulam, cloransulam-methyl, diclosulam, florasulam, flucarbazone and its salts, flumetsulam, metosulam, orthosulfamuron, penoxsulam, pyroxsulam, propoxycarbazone and its salts, pyribenzoxim, pyriftalid, pyriminobac-methyl, pyrimisulfan, pyrithiobac and its salts, pyroxisulam, thiencarbazone, thiencarbazone-methyl, and triafamone.

[0106] Examples of amino acid compounds include bialaphos and its salts, glufosinate and its salts, glufosinate P and its salts, and glyphosate and its salts.

[0107] Examples of the cyclohexanedione compounds include alloxydim, butroxydim, clethodim, cloproxydim, cycloxydim, propoxydim, sethoxydim, tepraloxydim, and tralkoxydim.

[0108] Examples of acetamide compounds include napropamide, dimethachlor, petoxamide, acetochlor, alachlor, allidochlor (CDAA), butenachlor, delaclor, diethatylethyl, propisochlor, pirinachlor, butachlor, dimethenamid, dimethenamid P, metazachlor, metolachlor, S-metolachlor, pretilachlor, propachlor, thenylchlor, flufenacet, and mefenacet.

[0109] Examples of bipyridylium compounds include cyperquat, morphamquat, diquat, and paraquat.

[0110] Examples of allyloxyphenoxypropionic acid compounds include clodinafop, clodinafop propargyl, clofop, cyhalofop butyl, diclofop, diclofop methyl, diclofop P methyl, fenoxaprop, fenoxaprop ethyl, fenoxaprop P ethyl, fluazifop, fluazifop butyl, fluazifop P butyl, haloxyfop, haloxyfop methyl, haloxyfop P methyl, isoxapiripop, metamifop, propaquizafop, quizalofop, quizalofop ethyl, quizalofop P ethyl, and quizalofop P tefuryl.

[0111] Carbamate compounds include asulam, carbetamide, desmedipham, chlorprocarb, phenisopham, cycloate, dimepiperate, pebulate, thiocarbazil, vernalate, barban, chlorbufam, chlorpropham, propham, swep, phenmedipham, butyrate, EPTC, esprocarb, molinate, orbencarb, prosulfocarb, pyributicarb, thiobencarb (benthiocarb), and triallate.

[0112] Examples of pyridine compounds include aminopyralid, clopyralid, diflufenican, dithiopyr, fluridone, fluroxypyr, haloxifene, florpyrauxifene, picloram and its salts, picolinafen, thiazopyr, and triclopyr and its salts.

[0113] Examples of urea compounds include benzthiazolone, bromuron, buturon, chlorbromuron, chloroxuron, difenoxuron, dimefuron, ethidimuron, fenuron, fluothiuron, metobenzuron, metobromuron, metoxuron, monolinuron, monuron (CMU), nebron, parafluron, siduron, thiazafluron, chlorotoluron, dymron, diuron (DCMU), fluometuron, isoproturon, linuron, methabenzthiazuron, tebuthiuron, cumyluron, carbutilate, and isouron.

[0114] Dinitroaniline compounds include benfluralin (beslodin), butralin, dinitramine, ethalfluralin, fluchloralin, isopropaline, nitralin, profluralin, oryzalin, pendimethalin, prodiamine, and trifluralin.

[0115] Examples of protoporphyrinogen oxidase (PPO) inhibitors include acifluorfen, aclonifen, azafenidin, bifenox, clomethoxynil, ethoxyfene, ethoxyfen-ethyl, fomesafen, fluazolate, fluoroglycofen, fluoroglycofen-ethyl, halosafen, lactofen, oxyfluorfen, butafenacil, epirifenacil, chlornitrofen (CNP), fluorodifen, fluoronitrofen (CFNP), nitrofen (NIP), oxiflufen, chlorphthalim, flumipropine, carfentrazone, carfentrazone-ethyl, cinidon-ethyl, flumiclorac pentyl, flumioxazin, fluthiacet, fluthiacet-methyl, oxadiargyl, oxadiazone, pentoxazone, pyraclonil, pyraflufen, pyraflufen-ethyl, saflufenacil, sulfentrazone, thidiazimine, benzfendizone, profluazole, and flufenpyr-ethyl.

[0116] Phenoxyacetic acid compounds include 2,4,5-T, 2,4-D and their salts, 2,4-DB and its salts, clomeprop, dichlorprop, fenoprop, MCPA and its salts, MCPB and its salts, mecoprop (MCPP) and its salts, and mecoprop P and its salts.

[0117] Hydroxyphenylpyruvate dioxygenase enzyme (HPPD) inhibitor compounds include benzobicyclon, benzofenap, bicyclopyrone, isoxaflutole, mesotrione, pyrasulfotole, pyrazolinate (pyrazolate), pyrazoxyfen, sulcotrione, tefuryltrione, tembotrione, topramezone, fenquinotrione, and tolpyralate.

[0118] Examples of triazine compounds include atraton, adiprothrin, chlorazine, cyprazine, desmetrin, dipropetrin, eglinadin ethyl, ipazine, metoprothrin, procyazine, proglinadin, prometon, propazine, sebutylazine, secbumeton, terbumeton, trietazine, ametryn, atrazine, cyanazine, dimethametryn, hexazinone, indaziflam, metamitron, metribuzin, prometryn, simazine (CAT), simetryn, terbuthylazine, terbutryn, and triaziflam.

[0119] Other compounds used as herbicides include amicarbazone, ethiozin, isomethiozin, aminocyclopyrachlor, aminotriazole, anilofos, piperophos, beflubutamid, benazolin, benfuresate, bentazon, bromacil, isosyl, bromobutide, bromofenoxime, bromoxynil, butamiphos, DMPA, TCTP (chlorthal dimethyl), cafenstrole, chloridazon (PAC), brompyrazone, chlorthal, clomazone, cumyluron, dicamba (MDBA) and its salts, chloramben, TCBA (2,3,8-TBA), benazolin ethyl, chlorfenac, chlorfenprop, dichlobenil (DBN), chlorthiamid (DCBN), cinmethylin, methiozolin, amitrole, flamproprop M, fosamine, methyldymron, monalid, MSMA, difenzoquat, diflufenzopyr, endothal and its salts, ethofumesate, etobenzanide, fenoxasulfone, fentrazamide, flupoxam, fluorochloridone, fluoxam Rutamon, Indanophan, Tridiphane, Ioxynil, Ipfencarbazone, Isoxaben, Triazifuran, Lenacil, Methylarsonic Acid, Naptalam, Flurochloridone, Norflurazon, Oxaziclomefone, Pinoxaden, Chloranocryl Dicryl, Pentanochlor (CMMP), Propanil, Propyzamide, Pyridate, Pyroxasulfone, Promacil, Quinclorac, Quinmelac, Quinoclamine, Terbacil, Cyclopyril Molate, Florpyrauxifen-benzyl, Lancotrione and its salts, Cyclopyranil, Bixlozone, Tetflupirolimet, Dimesulfazate, Zinosam, Dinoseb (DNBP), DNOC, Dinoterb, Ethinofen, Medinoterb, DSMA, Cacodylic Acid, Diphenamide, Naproanilide, Tebutam, Bensulide, Dalapon, TCA, Mefluidide, Phenyclohexanone Fluidon, CAMA, thiafenacil, trifludimoxadine, rimisoxafen, fenpyrazone, dioxopyritrione, sipirafluone, bipyrazone, benquitrione, fluchloraminopyr, pyriflubenzoxim, flufenoximacil, iptriazopyride, flusulfinam, broclozone, indlauxpyr, icaforin, pyraquinate, tetrapion (flupropanate) and its salts, and d-limonene.

[0120] [Method for improving plant environmental stress tolerance] The environmental stress tolerance improver in this embodiment can be used in, for example, agricultural land or non-agricultural land such as fields, paddy fields, lawns, and orchards. Furthermore, the environmental stress tolerance improver in this embodiment can be used by any fertilization method, such as foliage spraying, mixing into water supply, soil spraying, injection into the subsoil using an injector, seed treatment including treatment of bulbs and tubers, and direct fertilization of plants. Therefore, the method for improving environmental stress tolerance in this embodiment includes the procedure of fertilizing using the above-described environmental stress tolerance improver.

[0121] Application by mixing into water supply is carried out, for example, by administering granules to the water supply to crops or to the surface water of paddy fields. In one example, the concentration of the active ingredient in the water supply is 0.5 to 500 mg / L, preferably 1 to 300 mg / L. When administered to the surface water of paddy fields, the amount of the active ingredient used is, for example, 0.5 to 5000 g, preferably 3 to 3000 g per 10 ares of paddy field.

[0122] For application by foliage or soil spray, for example, granules are applied to the planting hole or its surroundings when transplanting seedlings, or granules and wettable powders are applied to the seeds, plants, or the soil around the plants. It may also be preferable to mix the active ingredient with the soil after application to the soil. The amount of active ingredient used for foliage or soil surface spraying is 1 m per 1 m of agricultural or horticultural land. 2 For example, it is 0.5 to 5000 mg, preferably 3 to 3000 mg per unit area.

[0123] In seed treatment applications, the agent is attached to the seeds by mixing and stirring the wettable powder or dust with the seeds, or by immersing the seeds in a diluted wettable powder. Seed treatment also includes seed coating treatment. The amount of active ingredient used in seed treatment is, for example, 0.005 to 10,000 g, preferably 0.05 to 1,000 g, per 100 kg of seeds. Seeds treated with agricultural and horticultural agents can be used in the same way as regular seeds.

[0124] The concentration and amount used may vary depending on the formulation, application time, application method, application location, target crop, etc., and may be increased or decreased without adhering to the above ranges. As described above, compound (I) and its tautomers exhibit excellent effects of improving environmental stress tolerance in a wide range of plants.

[0125] [Use of environmental stress tolerance improvers] As described above, the environmental stress tolerance improver of the present embodiment exhibits an excellent effect of improving environmental stress tolerance in a treated plant.

[0126] 〔summary〕 As described above, the agent for improving environmental stress tolerance of a plant according to embodiment 1 of the present invention comprises, as an active ingredient, a compound represented by the following formula (I) or a tautomer thereof, or an agriculturally acceptable salt thereof: [ka] (In formula (I), R 1 and R 2 each independently represents a hydrogen atom or an alkyl group having 1 to 4 carbon atoms, and R 3 ~R 5 each independently represents an alkyl group having 1 to 4 carbon atoms.

[0127] Furthermore, in the agent for improving environmental stress tolerance of a plant according to Aspect 2 of the present invention, in Aspect 1, the compound represented by formula (I) is preferably ergothioneine.

[0128] Furthermore, the agent for improving plant environmental stress tolerance according to Aspect 3 of the present invention, in Aspect 1 or 2, preferably improves tolerance to at least one environmental stress selected from high temperature stress, low temperature stress, freezing stress, salt stress, excess nutrient stress, drought stress, excess water stress, ultraviolet stress, low light stress, and high light stress.

[0129] Furthermore, the plant environmental stress tolerance improver of Aspect 4 according to the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is a salt stress tolerance improver.

[0130] Furthermore, the plant environmental stress tolerance improver of Aspect 5 of the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is a drought stress tolerance improver.

[0131] Furthermore, the plant environmental stress tolerance improver of Aspect 6 according to the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is a high temperature stress tolerance improver.

[0132] Furthermore, the plant environmental stress tolerance improver of Aspect 7 of the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is an excess nutrient stress tolerance improver.

[0133] Furthermore, the plant environmental stress tolerance improver of Aspect 8 of the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is an excessive water stress tolerance improver.

[0134] Furthermore, the plant environmental stress tolerance improver of Aspect 9 according to the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is an ultraviolet stress tolerance improver.

[0135] Furthermore, the plant environmental stress tolerance improver of Aspect 10 according to the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is an intense light stress tolerance improver.

[0136] Furthermore, the plant environmental stress tolerance improver of Aspect 11 of the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is a freezing stress tolerance improver.

[0137] Furthermore, the plant environmental stress tolerance improver of Aspect 12 of the present invention is the same as in any one of Aspects 1 to 3, wherein the environmental stress tolerance improver is a low-temperature stress tolerance improver.

[0138] Furthermore, a method for improving environmental stress tolerance in a plant according to a thirteenth aspect of the present invention comprises treating a plant with the environmental stress tolerance improver according to any one of the first to twelfth aspects.

[0139] The following examples are provided to further explain the embodiments of the present invention. Of course, the present invention is not limited to the following examples, and various modifications are possible in detail. Furthermore, the present invention is not limited to the above-described embodiments, and various modifications are possible within the scope of the claims. Embodiments obtained by appropriately combining the technical means disclosed herein are also included in the technical scope of the present invention. Furthermore, all of the documents cited in this specification are incorporated by reference. [Example]

[0140] Hereinafter, the effect of the environmental stress resistance improver according to this embodiment will be demonstrated using L-(+)-ergothioneine. Note that, glycine betaine, which is a compound different from the environmental stress resistance improver according to this embodiment, will be used as a comparative compound below. Note that, in the following explanation, L-(+)-ergothioneine may be abbreviated as "EGT" and glycine betaine may be abbreviated as "GB."

[0141] [Evaluation Example 1] Comparison of tolerance effects against salt stress L-(+)-ergothioneine (Examples 1 and 2, Comparative Example 3) and glycine betaine (Comparative Examples 1 and 2, Comparative Example 4) were prepared to the concentrations shown in Table 1. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0142] Arabidopsis thaliana (Col-0) was seeded at three plants per well in a 24-well cell culture plate. A liquid medium containing 1% sucrose and 0.1% agar powder (by weight) was added to Murashige and Skoog medium (Fujifilm Wako Pure Chemical Industries, Ltd.), and 2 mL of the medium was placed in each well.

[0143] The plants were grown in a climate chamber set at a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. Light conditions were set at a light intensity of 5000 lx in the center under fluorescent light. Four days after sowing, EGT or GB was added to the plants to achieve the specified concentration, and 24 hours later, a sodium chloride solution was added to the plants to a final concentration of 100 mM to apply salt stress.

[0144] Ten days after sowing, the number of surviving plants was counted, and the plant mortality rate was evaluated as an index of physiological disorders. The evaluation results are shown in Table 1. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) = {1-(number of surviving plants / number of plants tested)} x 100 Environmental stress suppression rate (%) = {1 - (mortality rate in the test compound-treated area / mortality rate in the untreated area)} x 100 [Table 1]

[0145] As shown in Table 1, physiological disorders such as chlorosis were observed in Arabidopsis thaliana due to salt stress, with 75% of the tested Arabidopsis thaliana plants dying (Comparative Example 5), and treatment with GB did not suppress death due to salt stress (Comparative Examples 1 and 2). In contrast, treatment with EGT suppressed death due to salt stress, with the mortality rate increasing to 14% at 1 mM (Example 1) and 39% at 0.1 mM (Example 2).

[0146] [Evaluation Example 2] Comparison of tolerance effects against drought stress EGT (Example 3) was prepared to have the concentration shown in the following Table 2. A commercially available EGT was used, and pure water was used as the solvent.

[0147] Arabidopsis thaliana (Col-0) seeds were sown in plastic pots measuring 60 mm in diameter and 55 mm in height, with one plant per pot. Six pots were placed in a deep plastic dish measuring 160 mm in diameter and 28 mm in height. 45 mL of vermiculite, 22.5 mL of granular soil (Kumiai Gardening Soil), and 22.5 mL of vermiculite were added to the pots in this order.

[0148] The plants were grown in a climate chamber set at a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. Light conditions were set to a light intensity of 5000 lx at the center under fluorescent light. Water was supplied from the bottom, with the water level set to approximately 5 mm. 22 days after sowing, 50 mL of EGT was added, and 2 days later, water supply was stopped for 18 days to induce drought stress.

[0149] The number of surviving plants was counted 18 days after the water supply was cut off, and the plant mortality rate was evaluated as an index of physiological disorder. The evaluation results are shown in Table 2. The mortality rate and environmental stress suppression rate were calculated using the following formula. Mortality rate (%) = {1-(number of surviving plants / number of plants tested)} x 100 Environmental stress suppression rate (%) = {1 - (mortality rate in the test compound-treated area / mortality rate in the untreated area)} x 100 [Table 2]

[0150] As shown in Table 2, drought stress caused physiological disorders such as wilting and necrosis in Arabidopsis plants, and 50% of the tested Arabidopsis plants died (Comparative Example 7), whereas treatment with EGT allowed all Arabidopsis plants to survive (Example 3).

[0151] [Evaluation Example 3] Comparison of tolerance effects against drought stress EGT (Example 4) or GB (Comparative Example 9) was prepared to have the concentrations shown in the following Table 3. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0152] 90 mL of granular culture soil (Kumiai Gardening Culture Soil) was placed in a plastic pot with a diameter of 60 mm and a height of 55 mm, and one cotton plant (Tohoku Co., Ltd.) was sown per pot.

[0153] The plants were kept in a greenhouse at a room temperature of 25° C. 23 days after sowing, 50 mL of EGT or 50 mL of GB was added, and 4 days later, water supply was stopped for 4 days to apply drought stress.

[0154] Four days after the water supply was cut off, leaves were collected and photographed with a digital camera. The photographs were analyzed using image analysis software WinROOF (Mitani Shoji Co., Ltd.) to quantify the total leaf area and green leaf area.

[0155] The leaf necrosis rate was evaluated 4 days after water deprivation using the total leaf area and green leaf area. The evaluation results are shown in Table 3. The leaf necrosis rate and environmental stress suppression rate were calculated using the following formulas. Leaf necrosis rate (%) ={1-(green leaf area / total leaf area)}×100 Environmental stress suppression rate (%) = {1 - (necrosis rate of leaves in the test compound-treated group / necrosis rate of leaves in the untreated group)} x 100 [Table 3]

[0156] As shown in Table 3, drought stress caused physiological disorders such as wilting, chlorosis, and necrosis in cotton plants, with 52% of the leaves tested suffering from necrosis (Comparative Example 10), and treatment with GB did not suppress necrosis due to drought stress (Comparative Example 9). In contrast, treatment with EGT suppressed the necrosis rate due to drought stress to 26% (Example 4).

[0157] [Evaluation Example 4] Comparison of resistance effects against high temperature stress EGT (Example 5, Comparative Example 13) or GB (Comparative Example 12, Comparative Example 14) was prepared to have the concentrations shown in the following Table 4. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0158] 80 mL of culture soil (Hanagokoro Co., Ltd.) was placed in plastic pots 60 mm in diameter and 55 mm in height, and one Arabidopsis thaliana (Col-0) seed was sown per pot. Four pots were placed in deep plastic plates 160 mm in diameter and 28 mm in height.

[0159] The plants were grown in a climate chamber set at a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. Light conditions were set to a light intensity of 5000 lx at the center under fluorescent light. Water was supplied from the bottom, with the water level set to approximately 5 mm. 41 days after sowing, 50 mL of EGT or 50 mL of GB was added, and one day later, the plants were exposed to a 42°C environment for 3 hours to induce high-temperature stress.

[0160] The number of surviving plants was counted 12 days after the high temperature stress was applied, and the plant mortality rate was evaluated as an index of physiological damage. The evaluation results are shown in Table 4. The mortality rate and environmental stress suppression rate were calculated using the following formula. Mortality rate (%) = {1-(number of surviving plants / number of plants tested)} x 100 Environmental stress suppression rate (%) = {1 - (mortality rate in the test compound-treated area / mortality rate in the untreated area)} x 100 [Table 4]

[0161] As shown in Table 4, high temperature stress caused physiological disorders such as wilting and necrosis in Arabidopsis plants, with 75% of the plants dying (Comparative Example 15), and treatment with GB did not suppress the mortality rate due to high temperature stress (Comparative Example 12). In contrast, treatment with EGT suppressed the mortality rate due to high temperature stress to 25% (Example 5).

[0162] [Evaluation Example 5] Comparison of tolerance effects against excess nutrient stress EGT (Example 6) or GB (Comparative Example 17) was prepared to have the concentrations shown in the following Table 5. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0163] Arabidopsis thaliana (Col-0) seeds were sown in plastic pots measuring 60 mm in diameter and 55 mm in height, with one plant per pot. Four pots were placed in deep plastic dishes measuring 160 mm in diameter and 28 mm in height. 45 mL of vermiculite, 22.5 mL of granular soil (Kumiai Gardening Soil), and 22.5 mL of vermiculite were added to the pots in this order.

[0164] The plants were grown in a climate chamber set at a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. Light conditions were set so that the light intensity was 5000 lx at the center under fluorescent light. Water was supplied from the bottom, with the water level set to approximately 5 mm. 61 days after sowing, 50 mL of EGT or 50 mL of GB was added, and one day later, liquid fertilizer (HYPONeX, manufactured by Hyponex Japan Co., Ltd.) was applied at a 5-fold dilution to impart excess nutrient stress.

[0165] The number of wilted leaves was evaluated one day after applying excess nutrient stress. The evaluation results are shown in Table 5. The leaf wilting rate and environmental stress suppression rate were calculated using the following formulas. Leaf wilting rate (%) = (number of wilted leaves / total number of leaves on the tested plants) x 100 Environmental stress suppression rate (%) = {1 - (Wilting rate in the test compound-treated group / Wilting rate in the untreated group)} x 100 [Table 5]

[0166] As shown in Table 5, 100% of the Arabidopsis leaves tested under excess nutrient stress showed wilting (Comparative Example 18), and treatment with GB did not significantly suppress wilting due to excess nutrient stress (Comparative Example 17). In contrast, EGT-treated Arabidopsis leaves (Example 6) showed a lower wilting rate than GB-treated Arabidopsis leaves, demonstrating that leaf wilting due to excess nutrient stress was suppressed.

[0167] [Evaluation Example 6] Comparison of tolerance effects against drought stress EGT (Examples 7 and 8) or GB (Comparative Examples 20 and 21) was prepared to have the concentrations shown in Table 6. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0168] 150 mL of granular culture soil (Kumiai Gardening Culture Soil) was placed in a plastic pot measuring 60 mm square and 66 mm high, and one soybean plant was sown per pot.

[0169] The plants were kept in a greenhouse at a room temperature of 25° C. 23 days after sowing, 50 mL of EGT or 50 mL of GB was added, and then water supply was stopped for 7 days to apply drought stress.

[0170] Seven days after water supply was cut off, the number of dead leaves was counted and the leaf mortality rate was evaluated as an index of physiological disorders. The evaluation results are shown in Table 6. The leaf mortality rate and environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (number of dead leaves / total number of leaves on the tested plants) x 100 Environmental stress suppression rate (%) = {1 - (leaf mortality rate in the test compound-treated group / leaf mortality rate in the untreated group)} x 100 [Table 6]

[0171] As shown in Table 6, soybeans suffered physiological disorders such as leaf wilting and necrosis due to drought stress, with 62% of the leaves dying (Comparative Example 22), and treatment with GB did not suppress the mortality rate due to drought stress (Comparative Examples 20 and 21). In contrast, treatment with EGT suppressed the mortality rate due to drought stress to 55% at 0.1 mM (Example 8) and to 38% at 1.0 mM (Example 7).

[0172] [Evaluation Example 7] Comparison of tolerance effects against drought stress EGT (Example 9) or GB (Comparative Example 24) was prepared to have the concentrations shown in the following Table 7. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0173] 1 kg of granular soil (Kumiai horticultural soil) was placed in a plastic pot measuring 135 mm in diameter and 110 mm in height, and 5 radish plants (Akamaru Hatsuka) were sown per pot.

[0174] The plants were kept in a greenhouse at a room temperature of 25°C. 22 days after sowing, 50 mL of EGT or 50 mL of GB was added, and then watering was stopped for 7 days. After that, the plants were grown under watering for 7 days, and then watering was stopped for another 7 days to subject them to drought stress.

[0175] The number of dead leaves on radishes subjected to drought stress was counted, and the leaf mortality rate was evaluated as an index of physiological disorder. The evaluation results are shown in Table 7. The leaf mortality rate and environmental stress suppression rate were calculated using the following formula. Leaf mortality rate (%) = (number of dead leaves / total number of leaves on the tested plants) x 100 Environmental stress suppression rate (%) = {1 - (leaf mortality rate in the test compound-treated group / leaf mortality rate in the untreated group)} x 100 [Table 7]

[0176] As shown in Table 7, drought stress caused physiological disorders such as leaf wilting and necrosis in radish plants, with 59% of the leaves dying (Comparative Example 25), and treatment with GB did not suppress the rate of death due to drought stress (Comparative Example 24). In contrast, treatment with EGT suppressed the rate of death due to drought stress to 17% (Example 9).

[0177] [Evaluation Example 8] Comparison of tolerance effects against drought stress EGT (Example 10) or GB (Comparative Example 27) was prepared to have the concentrations shown in the following Table 8. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0178] One liter of nursery soil (Takii Seeds) was placed in plastic pots measuring 135 mm in diameter and 110 mm in height, and 100 mm square of turf grass (Korean grass) was spread per pot.

[0179] The plants were kept in a greenhouse at a room temperature of 25°C. Approximately one month after sodding, 12.5 mL of EGT or 12.5 mL of GB was added, and then watering was stopped for seven days. After seven days of cultivation under watering, watering was stopped again for another seven days to subject the plants to drought stress.

[0180] The number of dead leaves of the drought-stressed turfgrass was counted, and the leaf mortality rate was evaluated as an index of physiological disorders. The evaluation results are shown in Table 8. The leaf mortality rate and environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (number of dead leaves / total number of leaves on the tested plants) x 100 Environmental stress suppression rate (%) = {1 - (leaf mortality rate in the test compound-treated group / leaf mortality rate in the untreated group)} x 100 [Table 8]

[0181] As shown in Table 8, physiological disorders such as necrosis were observed in turfgrass due to drought stress, with 100% of the leaves tested dying (Comparative Example 28), and treatment with GB did not suppress the mortality rate due to drought stress (Comparative Example 27). In contrast, treatment with EGT suppressed the mortality rate due to drought stress to 35% (Example 10).

[0182] [Evaluation Example 9] Comparison of tolerance effects against excessive water stress EGT (Example 11, Comparative Example 31) or GB (Comparative Examples 30 and 32) was prepared to have the concentrations shown in the following Table 9. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0183] Five mL of pure water was added to 9 cm petri dishes lined with filter paper, and 12 rapeseed seeds were sown per dish. The seeds were kept in an artificial climate chamber set at a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The light conditions were set so that the light intensity was 5000 lx in the center under fluorescent light irradiation.

[0184] Six days after seeding, the pure water in the dish was removed, and then 5 mL of EGT or 5 mL of GB was added to the dish. One day later, 50 mL of pure water was added to the dish to apply excess water stress.

[0185] The number of surviving plants was counted 19 days after the application of excess water stress, and the plant mortality rate was evaluated as an index of physiological disorder. The evaluation results are shown in Table 9. The mortality rate and environmental stress suppression rate were calculated using the following formula. Mortality rate (%) = {1-(number of surviving plants / number of plants tested)} x 100 Environmental stress suppression rate (%) = {1 - (mortality rate in the test compound-treated area / mortality rate in the untreated area)} x 100 [Table 9]

[0186] As shown in Table 9, excessive water stress caused physiological disorders such as chlorosis in rapeseed, with 60% of the rapeseeds tested dying (Comparative Example 33), and treatment with GB did not suppress the mortality rate due to excessive water stress (Comparative Example 30). In contrast, treatment with EGT suppressed the mortality rate due to excessive water stress to 25% (Example 11).

[0187] [Evaluation Example 10] Comparison of resistance effects against ultraviolet stress EGT (Examples 12 and 13, Comparative Examples 37 and 38) or GB (Comparative Examples 35, 36, 39 and 40) was prepared to have the concentrations shown in Table 10. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0188] Five mL of pure water was added to 9 cm petri dishes lined with filter paper, and 10 wheat seeds were sown per dish. The seeds were kept in a climate chamber set at a room temperature of 22°C, with a 16-hour light and 8-hour dark period. The light conditions were set to a light intensity of 5000 lx in the center under fluorescent light.

[0189] Seven days after seeding, the pure water in the dish was removed, and 5 mL of EGT or 5 mL of GB was added to the dish. One day later, the dish was irradiated with an ultraviolet lamp (Toshiba, GL-15) until the ultraviolet radiation intensity at a wavelength of 254 nm reached 550 μW / cm. -2 The temperature was set to 100°C, and the specimens were exposed to UV light for 1 hour to give them UV stress.

[0190] Six days after UV stress, the number of dead leaves was counted and the leaf mortality rate was evaluated as an index of physiological damage. The evaluation results are shown in Table 10. The leaf mortality rate and environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (number of dead leaves / total number of leaves on the tested plants) x 100 Environmental stress suppression rate (%) = {1 - (leaf mortality rate in the test compound-treated group / leaf mortality rate in the untreated group)} x 100 [Table 10]

[0191] As shown in Table 10, UV stress caused physiological disorders such as chlorosis in wheat, with 53% of the test wheat leaves dying (Comparative Example 41), and treatment with GB did not significantly suppress the mortality rate due to UV stress (Comparative Examples 35 and 36). In contrast, wheat treated with EGT had a lower mortality rate than wheat treated with GB, with the mortality rate due to UV stress being suppressed to 34% at 0.1 mM (Example 13) and 23% at 1.0 mM (Example 12).

[0192] [Evaluation Example 11] Comparison of resistance effects against ultraviolet stress EGT (Examples 14 and 15, Comparative Examples 45 and 46) or GB (Comparative Examples 43, 44, 47 and 48) was prepared to have the concentrations shown in Table 11. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0193] Lawn grass (Korean grass) cut into 50 mm squares was placed on a petri dish and maintained in a greenhouse at a room temperature of 25°C. The grass was trimmed to a length of 10 mm. 10 mL of EGT or 10 mL of GB was added to each petri dish, and one day later, the ultraviolet radiation intensity at a wavelength of 254 nm was measured under irradiation with an ultraviolet lamp (Toshiba, GL-15) at 525 μW / cm. -2 The temperature was set to 100°C, and the specimens were exposed to UV light for 1 hour to give them UV stress.

[0194] Seven days after UV stress, the number of dead leaves was counted and the leaf mortality rate was evaluated as an index of physiological damage. The evaluation results are shown in Table 11. The leaf mortality rate and environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (number of dead leaves / total number of leaves on the tested plants) x 100 Environmental stress suppression rate (%) = {1 - (leaf mortality rate in the test compound-treated group / leaf mortality rate in the untreated group)} x 100 [Table 11]

[0195] As shown in Table 11, physiological disorders such as chlorosis were observed in turfgrass due to UV stress, with 63% of the leaves tested dying (Comparative Example 49), and treatment with GB did not substantially suppress the mortality rate due to UV stress (Comparative Examples 43 and 44). In contrast, the mortality rate of turfgrass treated with EGT was lower than that of turfgrass treated with GB, with the mortality rate due to UV stress being suppressed to 13% at 0.1 mM (Example 15) and 6% at 1.0 mM (Example 14).

[0196] [Evaluation Example 12] Comparison of resistance effects against strong light stress EGT (Example 16) or GB (Comparative Example 51) was prepared to have the concentrations shown in the following Table 12. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0197] 90 mL of culture soil (Hanagokoro Co., Ltd.) was placed in a plastic pot with a diameter of 60 mm and a height of 55 mm, and four Arabidopsis thaliana (Col-0) plants were sown per pot.

[0198] The plants were kept in a climate chamber set at a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. Light conditions were set so that the light intensity was 5000 lx in the center under fluorescent light. 43 days after sowing, 12.5 mL of EGT or 12.5 mL of GB was added, and one day later, the plants were placed under LED light (Esbaybulbs) with a light intensity of 2000 μmol / m -2 The light intensity was set to 1 / sec and the cells were exposed to high light stress for 24 hours.

[0199] The number of bleached leaves of Arabidopsis plants subjected to high light stress was counted, and the leaf bleaching rate was evaluated as an index of physiological disorders. The evaluation results are shown in Table 12. The leaf bleaching rate and environmental stress suppression rate were calculated using the following formulas. Leaf bleaching rate (%) = (number of bleached leaves / total number of leaves on the tested plants) x 100 Environmental stress suppression rate (%) = {1 - (chlorosis rate of leaves in the test compound-treated area / chlorosis rate of leaves in the untreated area)} x 100 [Table 12]

[0200] As shown in Table 12, strong light stress caused physiological disorders such as chlorosis in Arabidopsis, with 37% of the leaves of the tested Arabidopsis turning white (Comparative Example 52), and treatment with GB did not suppress leaf whitening due to strong light stress (Comparative Example 51). In contrast, treatment with EGT suppressed the leaf whitening rate due to strong light stress to 8% (Example 16).

[0201] [Evaluation Example 13] Comparison of resistance effects against freezing stress EGT (Example 17, Comparative Example 55) or GB (Comparative Examples 54 and 56) was prepared to have the concentrations shown in the following Table 13. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0202] Five mL of pure water was added to 9 cm petri dishes lined with filter paper, and 10 broccoli seeds (green volume) were sown per dish. The plants were kept in a climate chamber set at a room temperature of 22°C, with a 16-hour light and 8-hour dark period. The light conditions were set to a light intensity of 5000 lx in the center under fluorescent light.

[0203] On the sixth day after sowing, the pure water in the dish was removed, and then 5 mL of EGT or 5 mL of GB was added to the dish. 14 days later, the dish was exposed to a -20°C environment for 20 minutes, and one day later, the dish was exposed to a -20°C environment for another 20 minutes to subject it to freezing stress.

[0204] The number of surviving plants was counted 24 hours after the application of freezing stress, and the plant mortality rate was evaluated as an index of physiological damage. The evaluation results are shown in Table 13. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) = {1-(number of surviving plants / number of plants tested)} x 100 Environmental stress suppression rate (%) = {1 - (mortality rate in the test compound-treated area / mortality rate in the untreated area)} x 100 [Table 13]

[0205] As shown in Table 13, freezing stress caused physiological disorders such as stem breakage and necrosis in broccoli plants, with 86% of the plants dying (Comparative Example 57), and treatment with GB did not suppress the mortality rate due to freezing stress (Comparative Example 54). In contrast, treatment with EGT suppressed the mortality rate due to freezing stress to 38% (Example 17).

[0206] [Evaluation Example 14] Comparison of resistance effects against freezing stress EGT (Example 18, Comparative Example 60) or GB (Comparative Examples 59 and 61) was prepared to have the concentrations shown in the following Table 14. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0207] Five mL of pure water was added to 9 cm petri dishes lined with filter paper, and 10 strawberry (wild strawberry) seeds were sown per dish. The dishes were kept in a climate chamber set at a room temperature of 22°C, with a 16-hour light and 8-hour dark period. Light conditions were set to a light intensity of 5000 lx in the center under fluorescent light.

[0208] On the 15th day after seeding, the pure water in the dish was removed, and then 5 mL of EGT or 5 mL of GB was added to the dish. Nine days later, the dish was exposed to a -20°C environment for 20 minutes to apply freezing stress.

[0209] Three days after the application of freezing stress, the number of surviving plants was counted, and the plant mortality rate was evaluated as an index of physiological damage. The evaluation results are shown in Table 14. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) = {1-(number of surviving plants / number of plants tested)} x 100 Environmental stress suppression rate (%) = {1 - (mortality rate in the test compound-treated area / mortality rate in the untreated area)} x 100 [Table 14]

[0210] As shown in Table 14, freezing stress caused physiological disorders such as necrosis in strawberries, with 63% of the strawberries dying (Comparative Example 62), and treatment with GB did not suppress the mortality rate due to freezing stress (Comparative Example 59). In contrast, treatment with EGT suppressed the mortality rate due to freezing stress to 29% (Example 18).

[0211] [Evaluation Example 15] Comparison of tolerance effects against low temperature stress EGT (Examples 19 and 20, Comparative Examples 66 and 67) or GB (Comparative Examples 64, 65, 68 and 69) were prepared to have the concentrations shown in Table 15. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0212] 1 mL of pure water was added to 3.5 cm petri dishes lined with filter paper, and 5 arugula seeds were sown per dish. The seeds were kept in a climate chamber set at a room temperature of 22°C, with a 16-hour light and 8-hour dark period. The light conditions were set to a light intensity of 5000 lx in the center under fluorescent light.

[0213] Four days after seeding, the pure water in the dish was removed, and then 1 mL of EGT or 1 mL of GB was added to the dish. 24 hours later, the dish was exposed to a 4°C environment for 48 hours to apply low-temperature stress.

[0214] The number of wilted leaves of the arugula was evaluated 3 days after the application of low temperature stress. The evaluation results are shown in Table 15. The leaf wilting rate and environmental stress suppression rate were calculated using the following formulas. Leaf wilting rate (%) = (number of wilted leaves / total number of leaves on the tested plants) x 100 Environmental stress suppression rate (%) = {1 - (leaf wilting rate in the test compound-treated group / leaf wilting rate in the untreated group)} x 100 [Table 15]

[0215] As shown in Table 15, 67% of the arugula leaves tested under low temperature stress showed physiological wilting (Comparative Example 70), and treatment with GB did not significantly suppress the leaf wilting rate due to low temperature stress (Comparative Examples 64 and 65). In contrast, treatment with EGT suppressed the leaf wilting rate due to low temperature stress to 0% (Examples 19 and 20).

Claims

1. An agent for improving environmental stress tolerance of a plant, which is to be applied to a plant or soil surrounding a plant, comprising, as an active ingredient, a compound represented by the following formula (I) or a tautomer thereof, or an agriculturally acceptable salt thereof, 【Chemistry 1】 (In formula (I), R １ and R ２ each independently represents a hydrogen atom or an alkyl group having 1 to 4 carbon atoms; R ３ ~R ５ each independently represents an alkyl group having 1 to 4 carbon atoms. The agent for improving environmental stress tolerance of a plant, which improves tolerance to salt stress.

2. The agent for improving environmental stress tolerance according to claim 1, wherein the compound represented by formula (I) is ergothioneine.

3. A method for improving environmental stress tolerance in a plant, comprising treating the plant with the environmental stress tolerance improver according to claim 1 or 2.

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